Author + information
- Received January 14, 1993
- Revision received March 25, 1993
- Accepted March 26, 1993
- Published online October 1, 1993.
- Claude R. Benedict, MD, DPhil, FACC∗,1,
- Debra H. Weiner, MPH∗,
- David E. Johnstone, MD FACC†,
- Martial G. Bourassa, MD, FACC‡,
- Jalal K. Ghali, MD, FACC§,
- John Nicklas, MD, FACC∥,
- Philip Kirlin, MD, FACC¶,
- Barry Greenberg, MD, FACC∗∗,
- Miguel A. Quinones, MD, FACC††,
- Salim Yusuf, MBBS, DPhil, FRCP, FACC‡‡,
- The SOLVD investigators1,§§
- ↵∗Address for correspondence: Claude R. Benedict, MD, DPhil, Department of Internal Medicine, Division of Cardiology, University of Texas Medical School, 6431 Fannin MSB 6.039, Houston, Texas 77030.
Objectives. The aim of this study was to determine the differences in neurohumoral responses between patients with pulmonary congestion with and without impaired left ventricular ejection fraction.
Background. Previous studies have established the presence of neurohumoral activation in patients with congestive heart failure. It is not known whether the activation of these neurohumoral mechanisms is related to the impairment in systolic contractility.
Methods. The 898 patients recruited into the Studies of Left Ventricular Dysfunction (SOLVD) Registry substudy were examined to identify those patients with pulmonary congestion on chest X-ray film who had either unpaired (<- 45%, group I) or preserved (> 45%, group II) left ventricular ejection fraction. Plasma norepinephrine, plasma renin activity, arginine vasopressin and atrial natriuretic peptide levels were measured in these two groups of patients and compared with values in matched control subjects,
Results. Distribution of the New York Heart Association symptom classification was the same in the two groups of patients. Compared with control subjects, patients in group II with pulmonary congestion and preserved ejection fraction had no activation of the neurohumoral mechanisms, except for a small but statistically significant increase in arginine vasopressin and plasma renin activity. Compared with patients in group II, those in group I with pulmonary congestion and unpaired ejection fraction had significant increases in plasma norepinephrine (p < 0.002), plasma renin activity (p < 0.02) and atrial natriuretic peptide levels (p < 0.0007). When we controlled for baseline differences between groups I and II, the between-group differences in plasma norepinephrine (p < 0.02) and atrial natriuretic peptide (p < 0.002) remained significant. However, plasma renin activity was not significantly different between groups I and II. When the effects of diuretic agents and angiotensinconverting enzyme inhibitors were adjusted, patients with lower ejection fraction were found to have significantly higher plasma norepinephrine and atrial natriuretic peptide levels.
Conclusions. The results point to the importance of the decrease in left ventricular ejection fraction as one of the mechanisms for activation of neurohormones in patients with heart failure.
Milton Packer, MD, FACC, Chairman
↵§§ A complete list of the participating hospitals, central agencies and personnel involved in the SOLVD Registry study is provided in 10. Bangdiwala SI, Weiner DH, Bourasa MG, et al. Studies of Left Ventricular Dysfunction (SOLVD) Registry: rationale, design methods and description of baseline characteristics. Am J Cardiol 1992;70:347–353.
☆ This study was supported by contacts from Studies of Left Ventricular Dysfunction, Clinical Trials Branch, National Heart. Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland.
- Received January 14, 1993.
- Revision received March 25, 1993.
- Accepted March 26, 1993.